Current practice in forest tree breeding relies on phenotypic selection, a time-consuming process. Genetic analysis of woody plants is hindered by the long generation times, non-domestication, high levels of genetic diversity and large size of the plants in question. Additionally, little is known about the mode of inheritance for most traits of interest in forest trees. Tree breeding is made more difficult as, in addition to the long generation times, certain traits of interest such as wood properties change during growth and maturation. Methods that allow the early selection of genetically superior individual trees would be of value in programs to improve tree stock.
Isozyme markers have been used to explore genetic variation in forest tree populations. The method is limited, however, by the small number of enzymes for which assays are available (Conkle 1981). The scope of genetic analysis for forest trees was extended by the development of restriction fragment length polymorphisms (RFLPs). However, the analysis of RFLP markers is laborious and limiting.
In forest trees, the trait of disease resistance must be durable for individual trees to survive for decades and even centuries. In contrast, disease resistance in crop plants is often not durable. Qualitative, gene-for-gene resistance mechanisms are known for several crop species susceptible to rust diseases. Flor, Annu. Review Phytopathol. 9:275 (1971). In a gene-for-gene system, a discrete resistance gene in the host blocks infection by strains of the pathogen, except for pathogen strains carrying a specific virulence gene able to overcome the resistance gene. Virulence of a pathogen is the ability to overcome defense mechanisms in an otherwise resistant host. Major, discrete resistance genes are commonly overcome within a few years in agronomic crops where the pathogen's asexual repeating stage is present on the economically important host. Vanderplank, Host-Pathogen Interactions in Plant Disease (Academic Press, New York and London, 1982).
Inheritance of disease resistance in forest trees has been commonly explained by polygenic models where disease resistance is controlled by many genes, each with a small additive effect (see, e.g., Robinson, Host Management in Crop Pathosystems, MacMillan Publishing (1987), and von Weissenberg, Silva Fennica, 24(1):129-139 (1990)). Polygenic resistance was considered more likely to be durable in long-lived forest trees, and genetic analysis using inbred lines to detect discrete resistance genes was precluded by the long generation times and the high genetic load typical of forest trees.